Cardiac assist devices, commonly referred to as pacemakers, provide a wide range of functions but share a need to provide stimulus to the heart in order to initiate a heartbeat, to eliminate arrhythmia, or to defibrillate the heart. Traditional cardiac assist devices rely on electronic means to stimulate the heart and to monitor the presence of a normal or abnormal heartbeat. These devices typically use a battery as the source of electrical power, and much development effort has been expended in increased battery capacity and in improvements in the energy efficiency of the pacemaker systems. Further improvements in energy efficiency would benefit both the device manufacturer and the implant patient.
To the best of applicant's knowledge, none of the prior art cardiac assist devices provide means for achieving this efficiency goal. It is an object of this invention to provide an electrical stimulation system for improving the energy efficiency of a cardiac assist device by the use of pulsewidth modulation techniques that initiate cardiac excitation and contraction with signals having duty cycles far lower than one hundred percent.
Many prior art patents disclose means for sensing the response of a heart to the input from a pacemaker. Thus by way of illustration and not limitation, U.S. Pat. No. 5,957,857 discloses an improved automatic sensing system for an implantable pacemaker in which the sensing threshold is automatically set to optimally sense the P-wave or R-wave while rejecting noise. The invention of this patent is illustrative of traditional noise filtering and rejection techniques and addresses the need to sense heart function at a relatively low speed on the order of the second beat interval of the heart. The entire disclosure of this United States patent is hereby incorporated by reference into this specification.
U.S. Pat. No. 5,871,512 discloses the use of digital signal processing to detect specific signal artifacts sensed by a pacemaker, and the patent specifically relates to a movement of electrical potential in a negative direction. As with the foregoing U.S. Pat. No. 5,957,857, this measurement and analysis is done during a period in time after the entire pacing signal to the heart has been terminated. The entire disclosure of this United States patent is hereby incorporated by reference into this specification.
U.S. Pat. No. 5,330,512 deals in a similar fashion with the problem of measuring evoked potential caused by the heartbeat in the presence of much higher polarization potential in the cardiac tissues immediately disposed around the pacing electrodes. This patent further suggests the use of an additional electrode in a manner that permits the pacemaker system to make measurements of the electrical activity of myocardial tissue that are less susceptible to the effects of polarization potential. As with the foregoing patents, this patent restricts the application of its technique to a period (typically three milliseconds) following the pacing signal, which itself is typically about one millisecond in length. The entire disclosure of this U.S. patant is hereby incorporated by reference into this specification.
Thus, U.S. Pat. Nos. 5,957,857, 5,871,512, and 5,330,512 disclose improvements in sensing heart activity in an individual with an implanted pacemaker, operating in a frequency range that is consistent with the pacing signal (typically about 1 kilohertz) and with the heartbeat (typically about 1 hertz).
U.S. Pat. No. 5,782,880 discloses a low energy pacing waveform for an implantable pacemaker, and it suggests the use of a waveform different from the exponential decay waveform resulting from capacitator's discharge that is used in most pacemaker devices. This patent also discloses a pacing signal that is shaped so as to provide an adequate safety factor in reliably pacing the cardiac tissue but that reduces the energy required to do so. However, as with all other prior art devices, the device of the '880 patent utilizes a full-time signal over the approximate 1 millisecond pacing period. The entire disclosure of this patent is hereby incorporated into this specification.
Reference may also be had to texts dealing with the topic of cardiac pacing. Thus, e.g., a text entitled “Cardiac Pacing for the Clinician,” edited by M. Kusumoto and N. Goldschlager, Lippincott Williams & Wilkins, Philadelphia, Pa., 2001, contains several chapter sections that deal with the physiology of cardiac pacing and sensing, and that describe the methods used by contemporary manufacturers in dealing with the issues described above. In chapter 1 on page 9 of this text, the typical safety factors employed by physicians are described; these are a 2:1 safety factor for pacing signal voltage and a 3:1 safety factor for pacing signal duration. The text further teaches that the energy dissipated in a pacing signal is directly proportional to the duration of the signal and to the square of the voltage of this signal. Thus, typical practice results in a pacing signal that is 12-fold higher than a signal that would be adequate to initiate the heartbeat. This 12-fold excess is intended to provide a very reliable pacing system, but it also may result in unnecessary acute and chronic damage to cardiac tissue and in the wastage of a majority of the energy available in the pacemaker battery.
The above text further describes, on pages 12 and 13 thereof, the nature of the evoked potential that results from the heartbeat itself, and it describes both its typical magnitude (10 to 20 millivolts) and its typical slew rate (1 to 4 volts per second).
The text further describes, on pages 18 to 24, the typical electrode structure used in pacing the heart and in sensing heart activity electrically. There is a specific discussion of the ongoing debate relating to unipolar versus bipolar pacing employing the use of one or two electrodes external to the pacemaker case, respectively.
Furthermore, and again referring to the text “Cardiac Pacing for the Clinician,” (and specifically to FIG. 1.15 on page 22), it is disclosed that the stimulation threshold of the heart increases substantially after initial implantation and use. It is generally acknowledged that damage to sensitive cardiac tissues is one of the primary causes of this increase, which in requires higher pacing voltages and safety factors.
Prior art pacing systems rely on phenomena that are interpreted at the organ level, rather than the cellular or intracellular level. Thus, for instance, terms such as “capture” (describing the successful initiation of a heartbeat resulting from a pacing signal), and “refractory period” (describing the brief period following a successful pacing event during which a next heartbeat is impossible to induce with a typical pacing signal), are used to describe cause and effect at the level of the organ (in this case the heart). While there is a very well developed understanding in the literature and in the patent art of cellular-level phenomena, prior art devices have not taken advantage of this insight in the design of pacing systems. A review of the literature reveals that these cellular-level phenomena occur at speeds far faster than the timeframe of the heartbeat (1 second) or even a typical pacing signal (1 millisecond).
In an article entitled “Calcium Dynamics in the Extracellular Space of Mammalian Neural Tissue”, Biophysical Journal, Volume 76, Apr. 1999, pages 1856–1867, authors David M. Egelman and P. Read Montague describe the behavior of the calcium channel during neural activity. Specifically, in FIG. 7, it is disclosed that the change in calcium concentration over time reveals a time constant on the order of 10 to 20 microseconds during the process of nerve firing. A similar analysis of FIG. 5 shows a recovery period for calcium concentration having a time constant on the order of 40 microseconds. Thus, this experimental work reveals that the total time for both the upward and downward change in calcium concentration for an individual cell involved in nerve firing to be on the order of 50 microseconds. Further, the rise time of 10 to 20 microseconds is consistent with excitation frequencies on the order of 50 to 100 kilohertz, i.e., the response to external stimulus at the cellular level occurs approximately 50 to 100 times more quickly than the typical 1 millisecond cardiac pacing signal and approximately 50,000 to 100,000 more quickly than the typical pulse rate.
More recent developments in electronic tissue stimulation systems have led to use of implantable deep brain stimulation (DBS) systems to treat essential tremor, Parkinson's disease, and epilepsy. Other advances have led to implantable vagal nerve stimulation systems to treat chronic pain. These systems share the basic attribute of stimulating brain tissue (DBS) or nerve tissue (pain therapy) with cardiac pacing systems. As a result the same benefits of this invention accrue to them as well.
It is one object of this invention to provide a cardiac assist process which takes advantage of the speed of cellular response to external stimuli, and which is substantially more energy efficient than prior art cardiac assist processes.
It is another object of this invention to provide a deep brain stimulation process which takes advantage of the speed of cellular response to external stimuli, and which is substantially more energy efficient than prior art deep brain stimulation processes.
It is a further object of this invention to provide a nerve stimulation process which takes advantage of the speed of cellular response to external stimuli, and which is substantially more energy efficient than prior art nerve stimulation processes.